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http://purl.uniprot.org/citations/29405337http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29405337http://www.w3.org/2000/01/rdf-schema#comment"

Aims

Glutamate neurotoxicity plays an important role in the pathogenesis of various neurodegenerative disorders. Many studies have demonstrated that glutamate transporter-1 (GLT-1), the dominant astrocytic glutamate transporter, is significantly reduced in the cerebral cortex of patients with Alzheimer's disease (AD), suggesting that glutamate-mediated excitotoxicity might contribute to the pathogenesis of AD. In a previous study, we have demonstrated marked alterations in the expression of the astrocytic water channel protein aquaporin-4 (AQP4) in relation to amyloid β deposition in human AD brains. As a functional complex, GLT-1 and AQP4 in astrocytes may play a neuroprotective role in the progression of AD pathology. However, few studies have examined the correlation between the expression of GLT-1 and that of AQP4 in human AD brain.

Methods

Here, using immunohistochemistry with antibodies against GLT-1 and AQP4, we studied the expression levels and distribution patterns of GLT-1 in areas showing various patterns of AQP4 expression in autopsied temporal lobes from eight patients with AD and five controls without neurological disorders.

Results

GLT-1 staining in the control group was present throughout the neocortex as uniform neuropil staining with co-localized AQP4. The AD group showed a significant reduction in GLT-1 expression, whereas cortical AQP4 immunoreactivity was more intense in the AD group than in the control group. There were two different patterns of GLT-1 and AQP4 expression in the AD group: (i) uneven GLT-1 expression in the neuropil where diffuse but intense AQP4 expression was evident, and (ii) senile plaque-like co-expression of GLT-1 and AQP4.

Conclusions

These findings suggest disruption of glutamate/water homoeostasis in the AD brain."xsd:string
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http://purl.uniprot.org/citations/29405337http://purl.uniprot.org/core/author"Yamamoto T."xsd:string
http://purl.uniprot.org/citations/29405337http://purl.uniprot.org/core/author"Ugawa Y."xsd:string
http://purl.uniprot.org/citations/29405337http://purl.uniprot.org/core/author"Tada M."xsd:string
http://purl.uniprot.org/citations/29405337http://purl.uniprot.org/core/author"Kakita A."xsd:string
http://purl.uniprot.org/citations/29405337http://purl.uniprot.org/core/author"Tsunoda A."xsd:string
http://purl.uniprot.org/citations/29405337http://purl.uniprot.org/core/author"Hoshi A."xsd:string
http://purl.uniprot.org/citations/29405337http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/29405337http://purl.uniprot.org/core/name"Neuropathol Appl Neurobiol"xsd:string
http://purl.uniprot.org/citations/29405337http://purl.uniprot.org/core/pages"628-638"xsd:string
http://purl.uniprot.org/citations/29405337http://purl.uniprot.org/core/title"Altered expression of glutamate transporter-1 and water channel protein aquaporin-4 in human temporal cortex with Alzheimer's disease."xsd:string
http://purl.uniprot.org/citations/29405337http://purl.uniprot.org/core/volume"44"xsd:string
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